We propose, in two phases of work, to follow up our initial observation that five previously isolated mutants of the nematode Caenorhabditis elegans show significant deficits of an apparent acetylcholine receptor (the mutants are resistant to the cholinergic agonist levamisole, and the apparent receptor is identified by its binding of the potent congener, m-aminolevamisole). In phase one we will improve the current assay for the apparent receptor and will screen many more of the available levamisole resistant C. elegans mutants (now numbering 329) for binding dificits. We will also try to develop an assay for detergent-solubilized binding, and we will search for mutants which overproduce the apparent receptor. In phase two, we will first determine which of the 13 genes containng such mutants are probable structural genes for components of the apparent receptor. We will then examine the consequences of primary mutational deficiencies in the apparent receptor for several aspects of cholinergic synapse formation and maintenance (including levels of cholinergic enzymes and synapse morphology. Finally we will attempt to puprify the apparent receptor for the eventual goal of generating monoclonal antibodies against it.